OBJECTIVES To describe a single institutional experience managing fetuses with supraventricular tachycardia (SVT) and to identify associations between patient characteristics and fetal and postnatal outcomes. BACKGROUND Sustained fetal SVT is associated with significant morbidity and mortality if untreated, yet the optimal management strategy remains unclear. METHODS Retrospective cohort study including fetuses diagnosed with sustained SVT (&gt;50% of the diagnostic echocardiogram) between 1985 and 2018. Fetuses with congenital heart disease were excluded. RESULTS Sustained SVT was diagnosed in 65 fetuses at a median gestational age of 30 weeks (range, 14-37). Atrioventricular re-entrant tachycardia and atrial flutter were the most common diagnoses, seen in 41 and 16 cases, respectively. Moderate/severe ventricular dysfunction was present in 20 fetuses, and hydrops fetalis was present in 13. Of the 57 fetuses initiated on transplacental drug therapy, 47 received digoxin first-line, yet 39 of 57 (68%) required advanced therapy with sotalol, flecainide, or amiodarone. Rate or rhythm control was achieved in 47 of 57 treated fetuses. There were no cases of intrauterine fetal demise. Later gestational age at fetal diagnosis (odds ratio [OR], 1.1, 95% confidence interval [CI], 1.01-1.2, P?=?.02) and moderate/severe fetal ventricular dysfunction (OR, 6.1, 95% CI, 1.7-21.6, P?=?.005) were associated with postnatal SVT. Two postnatal deaths occurred. CONCLUSIONS Fetuses with structurally normal hearts and sustained SVT can be effectively managed with transplacental drug therapy with minimal risk of intrauterine fetal demise. Treatment requires multiple antiarrhythmic agents in over half of cases. Later gestational age at fetal diagnosis and the presence of depressed fetal ventricular function, but not hydrops, predict postnatal arrhythmia burden. © 2020 Wiley Periodicals, Inc.OBJECTIVE Birth outcomes of women with anorexia nervosa are poorly understood. We hypothesized that hospitalization for anorexia nervosa before or during pregnancy is associated with an elevated risk of adverse maternal and infant birth outcomes. METHOD We performed a retrospective cohort study of 2,134,945 pregnancies in Quebec, Canada, from 1989 to 2016. https://www.selleckchem.com/products/fluzoparib.html The main exposure measure was anorexia nervosa requiring hospital treatment before or during pregnancy. Outcome measures included stillbirth, preterm birth, low birth weight, small-for-gestational age birth, preeclampsia, gestational diabetes, cesarean delivery, and other pregnancy disorders. We computed risk ratios and 95% confidence intervals (CI) for the association between anorexia nervosa and birth outcomes adjusted for maternal characteristics. RESULTS Compared with no hospitalization, anorexia nervosa hospitalization was associated with 1.99 times the risk of stillbirth (95% CI 1.20-3.30), 1.32 times the risk of preterm birth (95% CI 1.13-1.55), 1.69 times the risk of low birth weight (95% CI 1.44-1.99), and 1.52 times the risk of small-for-gestational age birth (95% CI 1.35-1.72). The associations with low birth weight and small-for-gestational age birth were more prominent in women hospitalized for anorexia nervosa during pregnancy or within 2?years of delivery. Hospitalization for anorexia nervosa was associated with certain maternal outcomes, including precipitate labor, acute liver failure, and admission to an intensive care unit. DISCUSSION Hospitalization for anorexia nervosa before or during pregnancy is associated with adverse infant and maternal outcomes. Infants are primarily at risk of stillbirth, preterm birth, low birth weight, and small-for-gestational age birth. © 2020 Wiley Periodicals, Inc.Hypoxia inactivates hypoxia-inducible factor (HIF) prolyl 4-hydroxylases (HIF-P4Hs), which stabilize HIF and upregulate genes to restore tissue oxygenation. HIF-P4Hs can also be inhibited by small molecules studied in clinical trials for renal anemia. Knowledge of systemic long-term inactivation of HIF-P4Hs is limited but crucial, since HIF overexpression is associated with cancers. We aimed to determine the effects of systemic genetic inhibition of the most abundant isoenzyme HIF prolyl 4-hydroxylase-2 (HIF-P4H-2)/PHD2/EglN1 on life span and tissue homeostasis in aged mice. Our data showed no difference between wild-type and HIF-P4H-2-deficient mice in the average age reached. There were several differences, however, in the primary causes of death and comorbidities, the HIF-P4H-2-deficient mice having less inflammation, liver diseases, including cancer, and myocardial infarctions, and not developing anemia. No increased cancer incidence was observed due to HIF-P4H-2-deficiency. These data suggest that chronic inactivation of HIF-P4H-2 is not harmful but rather improves the quality of life in senescence. © 2020 Federation of American Societies for Experimental Biology.Clinical dose of doxorubicin (100?nM) induced cellular senescence and various secretory phenotypes in breast cancer and normal epithelial cells. Herein, we reported the detailed mechanism underlying ginsenoside Rh2-mediated NF-κB inhibition, and mitophagy promotion were evaluated by antibody array assay, western blotting analysis, and immunocytostaining. Ginsenoside Rh2 suppressed the protein levels of TRAF6, p62, phosphorylated IKK, and IκB, which consequently inactivated NF-κB activity. Rh2-mediated secretory phenotype was delineated by the suppressed IL-8 secretion. Senescent epithelial cells showed increased level of reactive oxygen species (ROS), which was significantly abrogated by Rh2, with upregulation on SIRT 3 and SIRT 5 and subsequent increase in SOD1 and SOD2. Rh2 remarkably favored mitophagy by the increased expressions of PINK1 and Parkin and decreased level of PGC-1α. A decreased secretion of IL-8 challenged by mitophagy inhibitor Mdivi-1 with an NF-κB luciferase system was confirmed. Importantly, secretory senescent epithelial cells promoted the breast cancer (MCF-7) proliferation while decreased the survival of normal epithelial cells demonstrated by co-culture system, which was remarkably alleviated by ginsenoside Rh2 treatment. These data included ginsenoside Rh2 regulated ROS and mitochondrial autophagy, which were in large part attributed to secretory phenotype of senescent breast epithelial cells induced by doxorubicin. These findings also suggested that ginsenoside Rh2 is a potential treatment candidate for the attenuation of aging related disease. © 2020 John Wiley &amp; Sons, Ltd.